Patients with hypertrophic cardiomyopathy (HCM) exhibit abnormalities in coronary flow response to stress stimuli such as pacing and ergonovine, and the vasodilator, dipyridamole. These stimuli often elicit anginal chest pain in such patients. It has therefore been suggested that patients with HCM have decreased small coronary vasodilator reserve. To determine if this phenomenon applied to other vascular beds, we studied the forearm vasodilator capacity using ischemia (occlusion of the circulation) as the vasodilator stimulus. We found that patients with HCM in fact do have decreased vasodilator capacity in their forearm vasculature compared to normals. This is manifested by a decreased peak flow and increased vascular resistance at various durations of ischemia, compared to normals. This suggests that patients with HCM may have an abnormality of smooth muscle regulation that affects both the myocardial and peripheral vasculature.